We plan to delineate further the interrelatignships of PTH, 1,25-(OH)2D3 and phosphate with respect to their effect of 25-OHD3-1alpha-hydroxylase to PTH will be determined during different degrees of vitamin D-deprivation. The mechanism by which small changes in vitamin D status can alter the extant activity of 25-OHD3-1alpha-hydroxylase and it's respofse to increased levels of circulating PTH has not been defined. An increase in circulating PTH and, in the absence of increased levels of circulating PTH, hypophosphatemia, both can be major determinants of the increased activity of 25-OHD3-1alpha-hydroxylase characteristic of the vitamin D-deficient state. To determine whether the effect of vitamin D status on the response of 25-OHD3-1alpha-hydroxylase to parathyroid hormone is modulated by a change in phosphate status, the response of 25-OHD3-1alpha-hydroxylase to increased levels of circulating PTH during varying degrees of vitamin D-deprivation, will be determined in chicks on a normal phosphate diet and in chicks on a low phosphate diet. In the chicks on a low phosphate diet, if 25-OHD3-1alpha-hydroxylase becomes responsive to PTH at lesser degrees of vitamin D-deprivation, this would suggest that phosphate depletion does play a critical role in determining the responsiveness of 25-OHD3-1alpha-hydroxylase to PTH at a given level of vitamin D status.